Snakebite cases are not unusual to ED visit across the globe. Snakebite is an acute life-threatening time limiting medical emergency. It is a preventable public health hazard often faced by rural population in tropical and subtropical countries with heavy rainfall and humid climate. Although death due to snakebite is disproportionately low to the number of total bites partly because of bite by a non-venomous breed or dry bite (bites not accompanied by the injection of venom). Over 3000 species of snakes have been identified worldwide, with nearly 800 species considered venomous. In Indian subcontinent there are more than two hundred species of snakes out of which only about one-third will be venomous.

The three major families of venomous snakes are the Elapidae, the Viperidae, and the Colubridae Hydrophidae (WHO 2010).

Elapidae (cobra, king cobra, krait, and coral snake): Neuroparalytic toxin.

Viperidae (vipers): Vasculotoxic – Hemotoxic – bleeding disorder

Hydrophidae (sea snake): Though venomous, they seldom bite. Neuroparalytic toxin.

Whatever be the venom status of the biting snake all cases of such bite should get treated in a health care facility.

First aid and Transport of the victim

It aims to retard systemic absorption of venom and to prevent systemic effect of venom. It should be initiated as soon as the victim realizes about the bite before shifting to nearest medical facility. It is not mandatory to look for a fan mark to establish authentication of a bite.

Reassurance of the victim is important as it will ease the patient’s mental stress. Another important step in the pre-hospital setting is to immobilize the affected limb like in a case of a bone fracture. Any available rigid object can be used as a splint and to be tied with a roller bandage or a cloth. Nothing should be given orally. Traditional measures like tying a tourniquet or cutting and suctioning in an attempt to drain venom is to be discouraged. Patient should not be allowed to walk/run but should be passively transported as it will cause increased circulatory distribution of the venom. For every intervention adopted vital time should not be wasted.

Rapid clinical assessment and resuscitation

On arrival to the health care facility victim should be attended by a qualified physician with knowledge and experience to handle such cases. Many a times non-specific symptoms can lead to confusion because of anxious victim or bystanders. Definitive treatment with Anti-snake Venom (ASV) to be started as soon as signs of local/systemic envenomation begins. Hence knowledge of recognizing such signs and symptoms is necessary to efficiently treat such cases.

Symptomatic Patients

Neuroparalytic Venom mainly affects the neuro-muscular junction

Neuroparalytic snakebite patients present with typical symptoms within 30 min– 6 hours in case of Cobra bite and 6 – 24 hours for Krait bite. Although these time frame can vary significantly. These symptoms can be remembered as 5 Ds and 2 Ps.

5 Ds – Dyspnea, Dysphonia, Dysarthria, Diplopia, Dysphagia

2 Ps – Ptosis, Paralysis

Other signs are impending respiratory failure, diminished/lost tendon reflexes(DTR) and head lag.

Vasculotoxic toxidrome has both local and systemic manifestations. Locally there can be pain, swelling, blister formation or necrosis of the affected part. The swelling can be significant causing compartment syndrome. Hence surgical intervention is mandate early in the treatment as any delay can cause loss of the affected limb.

Systemic manifestation includes visible gingival bleed, epistaxis, ecchymosis, hematemesis, hemoptysis, hematochezia, sub-conjunctional bleed and bleeding from the bite mark per se. Acute abdominal pain can be attributed to gastro-intestinal or retro peritoneal bleed. Lateralizing neurological symptoms like asymmetrical pupils may point towards a Intra cranial bleed.

Life threatening complications are due to renal involvement. Patient presents with hematuria, hemoglobinuria, myoglobinuria followed by oliguria and anuria with acute kidney injury (AKI). Hypotension due to hypovolemia or vasodilatation or direct cardiotoxicity aggravates acute kidney injury. Long term sequelae e.g. pituitary insufficiency with Russell’s viper, Sheehan’s syndrome or amenorrhea in females.

Resuscitation and definitive urgent management should follow one the diagnosis is confirmed. The below mentioned are the red flag situations which require urgent resuscitation:

• Profound hypotension and shock resulting from direct cardiovascular effects of the venom or secondary effects such as hypovolemia, release of inflammatory vasoactive mediators, hemorrhagic shock or rarely primary anaphylaxis induced by the venom itself.
• Terminal respiratory failure from progressive neurotoxic envenoming that has led to paralysis of the respiratory muscles.
• Sudden deterioration or rapid development of severe systemic envenoming following the release of a tight tourniquet or compression bandage.
• Cardiac arrest precipitated by hyperkalemia resulting from skeletal muscle breakdown (rhabdomyolysis) after bites by sea snakes, certain kraits and Russell’s vipers.
• If the patient arrives late: Late results of severe envenoming such as renal failure and septicemia complicating local necrosis.

A very simple diagnostic tool: 20 mins whole blood clotting test (20WBCT) can give clue of hemolytic nature of toxin and warrants initiation of Anti-Snake Venom.

Anti-snake Venom (ASV)

Anti-snake venom is available is most of the health care facility where snake bite is prevalent. There is no absolute contradiction to ASV. Whenever indicated ASV should be started as soon as possible in indicated cases and has to be given in appropriate quantity. Commercially available ASV may be monovalent or polyvalent. In India polyvalent variant is only available which is effective against four common species; Russell’s viper, Common Cobra, Common Krait and Saw Scaled viper

ASV come in two forms: lyophilized powder and liquid. Lyophilized ASV is simply liquid ASV freeze-dried. Both the forms are equally potent in neutralizing venom. Advantage of lyophilized form against liquid is that the former has a longer shelf life and does not require a cold chain.

Dose of ASV:

ASV should be given only by the IV route, and should be given slowly, under supervision during the initial period to intervene immediately at the first sign of any reaction. The rate of infusion can be increased gradually in the absence of a reaction until the full starting dose has been administered. ASV must never be given by the IM route because of poor bioavailability by this route. Snakes inject the same dose of venom into children and adults. Children must therefore be given exactly the same dose of antivenom as adults. Epinephrine (adrenaline) should always be drawn up in readiness before ASV is administered.

Total ASV requirement ranges from 10 to 25 vials.

For neuroparalytic snakebite – ASV 10 vials stat as infusion over 30 minutes followed by 2nd dose of 10 vials after 1 hour if no improvement within 1st hour.

For vasculotoxic snakebite – Two regimens low dose infusion therapy and high dose intermittent bolus therapy can be used. Low dose infusion therapy is as effective as high dose intermittent bolus therapy and also saves scarce ASV doses.

Low Dose infusion therapy – 10 vials for Russel’s viper or 6 vials for saw scaled viper as stat as infusion over 30 minutes followed by 2 vials every 6 hours as infusion in 100 ml of normal saline till clotting time normalizes or for 3 days whichever is earlier.

Or

High dose intermittent bolus therapy – 10 vials of polyvalent ASV stat over 30 minutes as infusion, followed by 6 vials 6 hourly as bolus therapy till clotting time normalizes and/or local swelling subsides.

No ASV for Sea snakebite or pit viper bite as available ASV does not contain antibodies against them.

Adverse Anti Snake Venom Reactions Anaphylactic reaction to ASV is not managed correctly it can be treated in

an uncommon occurrence. However, if even remote health care facility. Early anaphylactic reactions occur within 10–180 min of start of therapy and is characterized by itching, urticaria, dry cough, nausea and vomiting, abdominal colic, diarrhea, tachycardia, and fever. Some patients may develop severe life-threatening anaphylaxis characterized by hypotension, bronchospasm, and angioedema.

Pyrogenic reactions usually develop 1–2 h after treatment. Symptoms include chills and rigors, fever, and hypotension. These reactions are caused by contamination of the ASV with pyrogens during the manufacturing process.

Late (serum sickness–type) reactions develop 1–12 (mean 7) days after treatment. Clinical features include fever, nausea, vomiting, diarrhea, itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy, immune complex nephritis and, rarely, encephalopathy.

At the first sign of a reaction we have to stop the ASV immediately. Administer Epinephrine (adrenaline) (1 in 1,000 solution, 0.5 mg (i.e 0.5 ml) in adults intramuscular over deltoid or over thigh; In children 0.01 mg/kg body weight) for early anaphylactic and pyrogenic ASV reactions. Ideally 2 syringes should be drawn up ready if the ASV is known to cause frequent reactions. Administer chlorpheniramine maleate 10 mg intravenously.

Late Serum sickness reactions can be easily treated with an oral steroid such as prednisolone, adults 5mg 6 hourly, oral H₁ antihistamines provide additional symptomatic relief.

Neurotoxic Envenomation

Antivenom treatment alone cannot be relied upon to save the life of a patient with bulbar and respiratory paralysis. Neostigmine is an anticholinesterase that prolongs the life of acetylcholine and can therefore reverse respiratory failure and neurotoxic symptoms. It is particularly effective for post synaptic neurotoxins such as those of the Cobra. There is some doubt over its usefulness against the pre-synaptic neurotoxin such as those of the Krait and the Russell ’s viper. However, it is worth trying in these cases. In all cases of neurotoxic envenomation, the “AN challenge Test” to be undertaken: Atropine 0.6mg followed by neostigmine (1.5mg) to be given IV stat and repeat dose of neostigmine 0.5 mg with atropine every 30 minutes for 5 doses. A fixed dose combination of Neostigmine and glycopyrrolate IV can also be used. Thereafter to be given as tapering dose at 1 hour, 2 hour, 6 hours and 12 hour. Majority of patients improve within first 5 doses. Patient need observation closely for 1 hour to determine if the neostigmine is effective. After 30 minutes, any improvement should be visible by an improvement in ptosis. Positive response to “AN” trial is measured as 50% or more recovery of the ptosis in one hour.

Renal Failure and ASV

Renal failure is a common complication of species such as Russell’s Viper. The contributory factors are intravascular hemolysis, DIC, direct nephrotoxicity and hypotension and rhabdomyolysis. Such patient will require renal replacement therapy.

Antibiotics and Tetanus Prophylaxis

Broad spectrum antibiotic coverage along with post exposure tetanus prophylaxis.

Debridement of Necrotic Tissue

Cellulitis and Compartment syndrome needs urgent surgical intervention and require surgeon opinion.

Follow-up

A snakebite victim discharged from the hospital should continue to be follow up. At the time of discharge patient should be advised to return to the emergency, if there is worsening of symptoms or signs such as evidence of bleeding, worsening of pain and swelling at the site of bite, difficulty in breathing, altered sensorium etc. The patients should also be explained about the signs and symptoms of serum sickness. (fever, joint pain, joint swelling) which may manifest after 5-10 days.

Reference:

Management of Snake Bite- MOH Government of India

Author:

Dr. Soumar Dutta, Consultant & Coordinator, Emergency Medicine (Narayana Superspeciality Hospital, Kamrup, Assam)

The post Snake Bite Protocol – An Indian Perspective appeared first on CCEM Journal.

Leptospirosis is a widespread and prevalent zoonotic disease. It occurs in both temperate and tropical regions; the incidence in the tropics is approximately 10 times higher than in temperate regions.In the tropics, leptospirosis is mainly a disease of poverty (including low education, poor housing, absence of sanitation, and poor income) [5]. It is acquired through occupational exposure (subsistence farming) and living in rodent-infested, flood-prone urban slums [6]. We report an unusual presentation of leptospirosis in a patient who presented to the Emergency Department (ED) with yellowish discoloration of the body and decreased urine output.

Introduction:

Leptospirosis is a widespread and prevalent zoonotic disease. It occurs in both temperate and tropical regions; the incidence in the tropics is approximately 10 times higher than in temperate regions [1]. Leptospirosis is an underreported disease, and there are no reliable global incidence figures. A modeling exercise by the World Health Organization’s (WHO’s) Leptospirosis Burden Epidemiology Group estimated that there were 873,000 cases worldwide annually with 48,600 deaths [2]. The organism infects a variety of both wild and domestic mammals, especially rodents, cattle, swine, dogs, horses, sheep, and goats. Rodents are the most important reservoirs for maintaining transmission in most settings.[3]. Human infection usually results from exposure to environmental sources, such as animal urine, contaminated water or soil, or infected animal tissue. Portals of entry include cuts or abraded skin, mucous membranes, or conjunctivae. The infection may rarely be acquired by ingestion of food contaminated with urine or via aerosols. Controversy exists as to whether Leptospira can penetrate the intact skin. [4]. We report an unusual presentation of leptospirosis in a patient who presented to the Emergency Department (ED) with yellowish discoration of the body and decreased urine output.

Case report:

A 35 years old male patient, farmer by occupation, presented in the ED with complaint of fever, nausea and vomiting for 6 days which was associated with history of yellowish discoloration of the body and decreased urine output. History of alcohol intake for the past 15 years was also present. The blood pressure was 130/80 mm of hg and PR was 110 bpm. General physical examination was remarkable for icterus and conjunctival suffusion. Systemic examination was apparently within normal limits(WNL). ABG was suggestive of metabolic acidosis ( Ph: 7.15, HCO3: 7, Pco2: 21, Na: 120, K: 2.8). ECG in the ED was WNL. Provisional diagnosis of leptospirosis, malaria and dengue was kept with due consideration to other atypical infections like scrub typhus and chikungunea fever. Patient was given empirical antibiotics (including coverage for leptospira) and antimalarials. Initial lab reports were suggestive of severe sepsis and hepatorenal dysfunction. (Refer to table 1). As per the lab reports the antibiotic support was escalated. Dengue (NS-1 antigen and Ig M) and malaria tests (Antigen and peripheral blood smear) were negative on day 2 of admission. Antimalarials were stopped. Howeveer despite antibiotic escalation there was progressive worsening of sepsis, renal and heatic dysfunction, although patient was hemodynamically stable. Serum procalcitonin was more than 75 IU/ml. In view of deranged renal function patient was given 2 sessions of hemodialysis. Final Blood and urine cultures reports did not show any growth of bacteria. In the mean time USG and later on CT abdomen (non contrast) reports were s/o acute pancreatitis. Conservative approach was followed.An upper GI endoscopy was done which revealed oesophageal candidiasis. Considering the critical state of the patient and non recovery of sepsis, a possibility of systemic fungal infection was kept and parentral antifungal agent (Mikafungin) was started. On day 5 leptospira Ig M report came to be positive. Chikungunea and scrub typhus (Weil Felix test) tests were negative. Gradually sepsis, renal and liver functions started resolving and patient was discharged with normal renal function and near normal liver function.

Table 1

Discussion:

In the tropics, leptospirosis is mainly a disease of poverty (including low education, poor housing, absence of sanitation, and poor income) [5]. It is acquired through occupational exposure (subsistence farming) and living in rodent-infested, flood-prone urban slums [6]. These are often associated with increased rainfall or flooding, which presumably increased the risk of exposure to contaminated water [7-11]. This case of leptospirosis was unusual because though the diagnosis of leptospirosis was straight forward clinically, the recovery was delayed because of underlying fungal infection. Leptospirosis presenting along with fungal infection is an unusual presentation.

REFERENCES:

1. Hartskeerl RA, Collares-Pereira M, Ellis WA. Emergence, control and re-emerging leptospirosis: dynamics of infection in the changing world. ClinMicrobiol Infect 2011; 17:494.
2. World Health Organization. Global burden of human leptospirosis and cross-sectoral interventions for its prevention and control. http://www.pmaconference.mahidol.ac.th/dmdocuments/2013-PMAC-Poster-P9-Bernadette%20Abela-Ridder.pdf (Accessed on August 13, 2013).
3. Ko AI, Goarant C, Picardeau M. Leptospira: the dawn of the molecular genetics era for an emerging zoonotic pathogen. Nat Rev Microbiol 2009; 7:736.
4. Stern EJ, Galloway R, Shadomy SV, et al. Outbreak of leptospirosis among Adventure Race participants in Florida, 2005. Clin Infect Dis 2010; 50:843.
5. Jesus MS, Silva LA, Lima KM, Fernandes OC. Cases distribution of leptospirosis in City of Manaus, State of Amazonas, Brazil, 2000-2010. Rev Soc Bras Med Trop 2012; 45:713.
6. Reis RB, Ribeiro GS, Felzemburgh RD, et al. Impact of environment and social gradient on Leptospira infection in urban slums. PLoSNegl Trop Dis 2008; 2:e228.
7. Kawaguchi L, Sengkeopraseuth B, Tsuyuoka R, et al. Seroprevalence of leptospirosis and risk factor analysis in flood-prone rural areas in Lao PDR. Am J Trop Med Hyg 2008; 78:957.

Author:

1. Dr. Shashank Gupta, Consultant Nephrologist (Narayana Superspeciality Hospital, Guwahati)
2. Dr. Apurba Kumar Borah, Consultant and HoD, Critical Care Medicine (Narayana Superspeciality Hospital, Guwahati)

The post An Unusual Case Of Leptospirosis: A Case Report appeared first on CCEM Journal.

Bartter’s Syndrome is characterized by renal potassium wasting with hypokalemia, metabolic alkalosis, increased renin-angiotensin-aldosterone system, normal blood pressure, resistance to the pressor effects of angiotensin II and juxtaglomerular cell hyperplasia. Most of the cases have been noted in the pediatric age group and adult-onset cases are very rare. In 1962, Frederic Bartter and his colleagues wrote their seminal paper based on two patients with hypokalaemic metabolic alkalosis, hyperaldosteronism, normal blood pressure, decreased pressor responsiveness to angiotensin II infusion and hyperplasia of the juxtaglomerular apparatus.The syndrome comprising the above mentioned observations was hence named after him. We report a case of adult-onset Bartter’s syndrome.

Case Report :

A 52 year old Gentleman with past history of Pulmonary Koch came with breathing difficulty along with fever.In view of severe respiratory distress, he was intubated and put on Mechanical Ventilation and treatment initiated after sending all relevant investigations.From history and from past medical records it was found that he was Normotensive in matters pertaining to his Blood Pressure.Initial  routine investigations revealed low serum Potassium levels for which intravenous Potassium Chloride was given. Despite correction,his serum Potassium did not rise and maintained in the range of 2.4-2.9 mEq/L.Hence cause for persistent hypokalemia was evaluated and Arterial Blood Gas analysis which was already being done to asses ventilatory status, correlated to look for any respiratory cause of hypokalemia.ABGs showed relatively persistent Metabolic Alkalosis.Obvious cause of Metabolic Alkalosis such as diueretics,renal failure were also ruled out.Ultrasonography of Abdomen revealed tiny Right renal calculi, hypoechoic  areas in bilateral Adrenal glands and Common Bile Duct Stone.In view of renal stone, urinary Calcium was evaluated which was found to be high.Suspecting Bartter Syndrome as the above mentioned findings pointed towards it, his serum Aldosterone level was assessed which was also high.Serum Renin levels were not assayed due to Laboratory constraints.Adrenal Biopsy was planned after patient stabilization in view of ?Adrenal Mass.Renal Biopsy was also not done.Meanwhile the patient was tracheostomised due to difficult weaning and subsequently the patient expired.

Discussion:

The constellation of Hypokalemia, Normotension, Metabolic Alkalosis, increased Aldosterone level and increased Urinary Calcium substantiated thedifferential  diagnosis of Bartter’s syndrome.However, as stated, Renin Activity could not be assesed and Renal Biopsy was not done.Also since Adrenal gland biopsy could not be done,an Adrenal glandtumour contributing to increased serum Aldosterone and hypokalemia could also be not ruled out.Hence  the possibility of any other differential diagnosis contributing to the above constellation of findings  is open for debate. Terms such as Bartter‐like syndrome do little to help the clinician identify the specific metabolic defect and treat the patient’s illness correctly. It may be better to sub‐classify Bartter syndrome by renal pathophysiological abnormality. By this method, Bartter syndrome falls into four subgroups: (i) antenatal Bartter syndrome (hyperprostaglandin E2 syndrome); (ii) the Gitleman variety of Bartter syndrome (Gitleman syndrome); (iii) classical Bartter syndrome; and (iv) pseudo‐Bartter syndrome.Often while assessing a cause of Hypokelemia we might miss that the hypokalemia  might represent anyone of the  constellation of findings correlating with any above mentioned syndrome.Bartter’s syndrome may be mimicked by magnesium deficiency, diuretic use or vomiting. Magnesium depletion causes kaliuresis, diuretics cause potassium and volume depletion and vomiting causes renal potassium wasting and volume depletion.The primary aim of the treatment of the Classical Bartter syndrome is correction of hypokalaemia and alkalosis. Therefore administration of potassium chloride is always necessary. The dose of KCl supplementation should individually be titrated in accordance to the patient’s needs and must balance the amount lost by the kidney. However, this mode of supplementation therapy is almost totally ineffective by itself, since administered potassium is lost through the kidney in a short period of time. It may seem logical that potassium‐sparing agents such as spironolactone  would be aneffective additiveto supplementation therapy at this stage. Indeed these groups of medication offer an effective but transient control of hypokalaemia.The most beneficial group of medication in treatment of classical Bartter syndrome is the prostaglandin synthetase inhibitors. Indomethacin (2–5 mg/kg/day), acetylsalicylic acid(100 mg/kg/day), and ibuprofen (30 mg/kg/day) have all been tried. But the most frequently used is indomethacin.

Conclusion:

Although rare a strong suspicion for this syndrome should be there while dealing with difficult cases of hypokalemia.

REFERENCES:

1. Bartter FC, Pronove P, Gill JR, Jr, MacCardle RC. Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis:a new syndrome. Am J Med. 1962;33:811. [PubMed]
2. Tomko DJ, Yeh BPY, Falls WF., Jr Bartter’s syndrome, Study of a 52-year-old man with evidence for a defect in proximal tubular sodium resorption and comments on therapy. Am J Med. 1976;61:111.[PubMed]
3. Gans ROB, Hoorntje SJ. Bartter’s syndrome. In: Cameron S, Davison AM, Grünfeld JP, Kerr D, Ritz E, editors. Oxford textbook of clinical nephrology. P. 782. Oxford University Press; 1992.
4. White MG. Bartter’s syndrome. Arch Intern Med. 1972;129:41. [PubMed]
5. Schöter J, Timmermans G, Sexberth HW, Greven J, Bachmann S. Marked reduction of Tamm-Horsfall protein synthesis in hyperprostaglandin E-syndrome. Kidney Int. 44:401, 1993. [PubMed]
6. Strokes JB. Effect of prostaglandin E2 on chloride transport across the rabbit thick ascending loop of Henle. Selective inhibition of the medullary portion. J Clinn Invest. 1979;64:495. [PMC free article][PubMed]
7. Halushka PV, Wohltmann H, PriviteraPj, Hurwitz G, Margolius HS. Bartter’s syndrome: urinary prostaglandin E-like material and kallikrein; Indomethacin effects. Ann Intern Med. 1977;87:281.[PubMed]
8. Stein JH. The pathogenetic spectrum of Bartter’s syndrome. Kidney Int. 1985;28:85. [PubMed]
9. Bartter FC. On the pathogenesis of Bartter’s syndrome. Miner Electrolyte Metab. 1980;3:61.
10. Baehler RW, Work J, Kotchen TA, McMorrow G, Guthrie G. Studies on the pathogensis of Bartter’s syndrome. Am J Med. 1980;69:933. [PubMed]

Author:

Dr. Dipankar Haloi, Fellow, Critical Care Medicine (IDCCM)

The post A Case of Adult-Onset Bartter’s Syndrome appeared first on CCEM Journal.

Introduction: The reported incidence of acute kidney injury after rhabdomyolysis is as high as 65%¹ which occurs as a result of multiple mechanisms including tubular obstruction, direct and ischemic tubular injury, or intrarenal vasoconstriction. In this report, we present a case of acute kidney injury induced by rhabdomyolysis in a young male post-trauma.

Presentation: A 37 yr old male patient presented to the emergency department with a history of trauma and physical assault 4 days back, multiple wounds all over the body and reduced urine output for 1 day. On examination he was found to have generalised swelling all over the body, multiple bruises and abrasions along with fracture of right 4^th metatarsal bone. Laboratory studies revealed CPK: 17345 IU/L; BUN: 79mg/dl; Serum creatinine: 11.35mg/dl; Serum potassium: 4.1meq/L; Urine Ph: 5. Adequate hydration was started with balanced salt solution and 0.9% NS also haemodialysis was done with which the patient’s renal functions improved gradually.

Conclusion: Rhabdomyolysis induced AKI in a patient with no co morbidities resolves gradually with adequate hydration and urine output monitoring.

Introduction:

Rhabdomyolysis is a clinical condition in which skeletal muscles break down rapidly releasing toxic substance like creatine kinase and myoglobin into the blood stream which in turn leads to kidney injury. This can happen because of sustained trauma, sepsis, heat stroke or even drugs.

Pathophysiology:

Rhabdomyolysis involves direct sarcolemic injury leading to depletion of ATP within the myocyte which impairs the function of ATPase pump. This causes an increased sarcoplasmic calcium levels leading to a state of persistent contraction of the myofibril. This sustained contraction leads to further energy depletion.

After myocyte injury, intracellular contents are released into the circulation.^{2, 3}   Hyperkalaemia, hyperuricaemia, and hyperphosphataemia can develop rapidly. High levels of phosphate released in blood; bind to calcium, and calcium–phosphate deposition occur in soft tissue, resulting into hypocalcaemia. Ischemic muscle is also forced to utilise anaerobic metabolism leading to metabolic acidosis.

During the recovery phase of rhabdomyolysis, significant number of patients develop hypercalcaemia, due to the release of vitamin D stores from injured muscle, providing substrate for the production of excess 1,25-dihydroxyvitamin D^4.  Hypercalcaemia may be further exacerbated if excess calcium is administered during the acute hypocalcaemic phase.

Myoglobin a dark red haem-containing protein stores and transports oxygen in muscle. Only small levels of it are normally present in plasma. It has a small molecular weight and is easily filtered. When the renal threshold for free myoglobin is exceeded it appears in urine.⁵ This then interacts with the Tamm–Horsfall proteins to form brown granular casts resulting in tubular obstruction. The process is favoured when the urine is acidic and may have no nephrotoxic effect when the urine is alkaline.

Myoglobin also causes deficit of nitric oxide leading to renal vasoconstriction which further compounds to kidney injury. Renal blood flow is further compromised by hypovolaemia, activation of the renin–angiotensin system, and additional vascular mediators. ²

Clinical features:

Severity of symptoms depends upon the degree of muscle damage and extent of kidney injury. Rhabdomyolysis may be asymptomatic or associated with muscle pain, nausea, sepsis, dyselectrolytemia, arrythmia, acute renal failure and even coma. A high degree of suspicion is needed from prompt management and avoidance of complications arising. Severe pain may at times limit limb movement and additionally in compartment syndrome or crush injury the muscles may get tense and swollen, leading to a sensoryneural loss. In diffuse muscle injury such as which occurs with drugs, there may be a generalised malaise with diffuse myalgia. Rarely, patients may volunteer that their urine has changed to a red or brown colour.

Lab findings:

Rhabdomyolysis is typically diagnosed when the CK is more than 5000 units/litre or five times its normal upper limit. Myoglobin levels peak before increases in CK, however, myoglobin is metabolised rapidly at sites outside of the kidney hence CK a more reliable marker of rhabdomyolysis. The absence of myoglobinuria does not rule out the possibility of rhabdomyolysis. In a study of 475 patients with rhabdomyolysis diagnosed by CK levels, myoglobinuria was only detected in 19%⁶  A Metabolic Acidosis with high anion gap is usually observed. Arterial blood gases also reveal trend of serum lactate and pH and serves as a guide for fluid replacement. Regular observations including hourly urine output are required to detect any deterioration promptly.

Case Report:

A 37 year old male, with no comorbidities, presented to the emergency department with complains of reduced urine output for 1 day, there was an associated history of physical assault 4 days back in which he suffered multiple contusions and abrasions all over his body along with a  fracture of right 4^th metatarsal bone, for which orthopaedic consult was taken. He was admitted to the critical care department and his initial laboratory studies revealed CPK: 17345 IU/L, BUN: 79mg/dl, Serum creatinine: 11.35mg/dl, Serum Potassium: 4.1meq/L, Urine Ph: 5, Serum Calcium: 7.2mg/dl, Serum Phosphorus: 7.6mg/dl.

Foley’s catheterization was done and central venous access was taken. Keeping myogologinuria induced rhabdomyolysis in mind he was thereafter managed primarily with fluid resuscitation with a target urine output of 3 ml/kg/hr or 300 ml/hr. 0.9% Normal saline, balanced salt solution was used while monitoring potassium and arterial blood gases to look for hyperchloraemic acidosis.

Continuous infusion of soda bicarbonate was initiated to alkalinise the urine to reduce the precipitation of Tamm–Horsfall protein complexes. A urinary pH of 7 was achieved on day 2 of the treatment. We also initiated infusion of Inj furosemide at 5-10 mg/hr to maintain an adequate urine output.

The patient was evaluated by a nephrologist and haemodialysis was initiated on day 2 and day 4 of admission, soda bicarbonate and furosemide was gradually tapered off with close monitoring of urine output. Fluid resuscitation continued, as guided by IVC dimensions. The patients renal functions improved gradually and he was later discharged in a stable condition with adequate urine output, with a serum creatinine of 2.59mg/dl and CPK: 150 IU/L.

Discussion:

We have reported a case of Acute kidney injury due to trauma induced rhabdomyolysis, patient here landed up into AKI due to dehydration and inadequate fluid resuscitation, which eventually resolved with intravenous hydration therapy. Another contributing factor of adequate recovery was young age of the patient with no history of any comorbidities or drug intake which could have been be a secondary cause of renal dysfunction.

Evidence for the use of sodium bicarbonate as a therapy to prevent AKI in rhabdomyolysis is lacking. A recent systematic review found no level 1–3 evidence to support its use.

Mannitol also has theoretical benefits by flushing nephrotoxic agents through the tubules, it extracts fluid that has accumulated in injured muscle, and acts as a free radical scavenger. Again there was no level 1–3 evidence to support the use of mannitol in the prevention of AKI^7.

Considering the benefit achieved by alkalising the urine and forced diuresis soda bi carbonate and furosemide infusion was used in this patient. Further studies may be needed to clarify this effect.

Hence, we conclude stating the primary treatment of Acute kidney injury induced by rhabdomyolysis being vigorous fluid resuscitation with intensive urine output monitoring.

References:

1. Meijer AR, Fikkers BG, Keijzer MH, Engelen BG, Drenth JP. Serum creatine kinase as predictor of clinical course in rhabdomyolysis: a 5-year intensive care survey. Intensive Care Med 2003; 29: 1121–5
2. Holt SG, Moore KP. Pathogenesis and treatment of renal dysfunction and rhabdomyolysis. Intensive Care Med 2001; 27: 803–11.
3. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009; 361: 62–72
4. Akmal M, Bishop J, Telfer N, Norman AW, Massry SG. Hypocalcaemia and hypercalcaemia in patients with rhabdomyolysis with and without acute renal failure. J Clin Endocrinol Metab 1986; 63: 137–42
5. David WS. Myoglobinuria. Neurol Clin 2000; 18: 215–43
6. Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicine (Baltimore) 2005; 84: 377–85
7. Scharman EJ, Troutman WG. Prevention of kidney injury following rhabdomyolysis: a systematic review. Ann Pharmacother 2013; 47: 90–105)

Abbreviations :

AKI : Acute Kidney Injury

CPK : Creatinine Phospho Kinase

CK : Creatinine Kinase

BUN : Blood Urea Nitrogen

ATP : Adenosine Tri Phosphate

NS : Normal Saline

IVC : Inferior Vena Cava

Author:

Dr. Sujan Dey, Consultant Critical Care, Artemis Hospitals, Gurugram.
Dr Reshma Tewari,Director Critical Care,Artemis Hospitals,Gurugram
Dr. Urvashi Modi, Registrar Critical Care, Artemis Hospitals, Gurugram.
Dr Muneer Jan,Assoc.Consultant Critical Care,Artemis Hospitals, Gurugram
Dr. Abhishek Goyal, Registrar Medicine, Artemis Hospitals, Gurugram.

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Respiratory tract infections are the most frequent of all the infections and account for the large number of workdays lost in the general population. Among them, pneumonia is the commonest disease with a high prevalence in the community and a cause of significant mortality and morbidity. Pneumonia is broadly defined as an infection of lung parenchyma [1]. Pneumonia is clinically divided into community-acquired pneumonia (CAP) and nosocomial pneumonia. Infectious Diseases Society of America (IDSA) defines CAP as “an acute infection of the pulmonary parenchyma that is associated with at least some symptoms of acute infection, accompanied by the presence of an acute infiltrate on a chest radiograph or auscultatory findings consistent with pneumonia in a patient not hospitalized or residing in a long-term care facility for more than 14 days before onset of symptoms” [2,3]. Aetiology of CAP is generally bacterial but the microbial pattern varies from place to place and so does the antimicrobial sensitivity and emerging resistance pattern. CAP is the leading cause of death in the world. But the seriousness of CAP, despite being a reasonably common and potentially lethal disease, often is underestimated by physicians and patients alike [4]. The treatment of CAP is complicated by growing threat of antimicrobial resistance and the tendency to rely on empirical therapy. Recent years have witnessed the emergence of new pathogens and also newer antibiotics designed to combat them [5]. Various studies have been done in different countries for example in Jordan [6], Thailand [7], New York [8] and Chile [9] regarding the microbial etiology and bacterial resistance. But there is limited published data describing microbiological causes of pneumonia in India [10]. Although a wide variety of recognized pathogens cause CAP, the precise etiology, pattern of microbial flora in various settings, antibiotic sensitivity and resistance in India is still not comprehensively studied. Our study is a sincere attempt to look into the microbiological  profile of the various causative agents of CAP and sensitivity pattern of organisms to plan therapy among patients in limited facility settings.

Materials and Methods:

It was a Hospital based Cross sectional study conducted in a tertiary care hospital in Guwahati, Assam. A total of 192 culture positive consecutive respiratory samples received in the Microbiology department of the hospital from August 2016 to July 2017 were included in the study. The study population were assessed for  symptoms, signs and laboratory data diagnostic of pneumonia.

Diagnosis was made on the basis of history, clinical examination, routine blood parameters (complete blood count, ESR) and chest radiograph. On diagnosis, samples were collected as per standard recommended protocols.  Respiratory samples included sputum, endotracheal tube aspirate, brochoalveolar lavage samples were collected before the patients received first course of antibiotics. The  samples thus obtained were sent for Gram staining and pyogenic culture and sensitivity to antibiotics.

Characterization of bacterial isolates:

The samples were aseptically inoculated on to Blood, Chocolate and Mac Conkey agar plates and incubated overnight at 37oC. Klebsiella pneumoniae (K.pneumoniae) isolates were identified by their morphology and biochemical characteristics.  Morphology  of   Klebsiella   identified   were large dome shaped colonies on Blood, Chocolate  agar  and lactose fermenting mucoid colonies on Mac Conkey agar. Gram staining revelaed  Gram  negative,  short,  stout,  blunt  rods. Negative Indole test, positive Voges-Proskauer test, positive Citrate utilization test, positive Urease test, acid and abundant gas production from glucose, lactose,  sucrose,  maltose  and mannitol sugar fermentation tests were the biochemical tests used in the interpretaion .

Antimicrobial Susceptibility Testing:

The isolates were screened for antimicrobial   susceptibility   testing   by   Kirby-Bauer   disc diffusion method on Mueller-Hinton agar (Hi-Media) and interpreted as per CLSI guidelines [7]. A  log  phase  broth culture inoculums of the isolate with a turbidity equivalent to McFarland 0.5 standard (1.5×10⁸ CFU/ml) was prepared and  lawn cultured on the Mueller-Hinton agar and allowed to dry. Antibiotic discs were applied to the Mueller  Hinton  agar  surface with the help of sterile forceps.  A panel  of antibiotics (Hi-media) as per the CLSI guidelines were selected . All  antibiotics  used  were  on  ATCC strains, to ensure satisfactory quality control.

The plates were then incubated at 37°C for 24 hours. Antimicrobial activity was indicated  by  an  inhibition  zone. The diameter of the  inhibition  zones  was  measured  in millimeter using a calibrated scale based on the CLSI guidelines and were tagged as sensitive or resistant.

Results:

In our study the most frequent pathogen was Klebsiella  pneumoniae (43.2%; n=83) followed by Pseudomonas aeruginosa (23%; n= 44)  and Staphylococcus aureus (10%; n= 19). Esherichia coli (7.8%;n= 15), Streptococcus pneumonaie (3.1%; n= 6) and Moraxella catarrhalis (2%; n=4) were the other organisms. For the Gram negative organisms causing pneumonia, most of them were sensitive to colistin followed by carbapenems (meropenem 90%) followed by aminoglycosides (amikacin 83%). Aminoglycosides (Tobramicin 100%), macrolides , quinolones and 3^rd generation cephalosporins showed good sensitivity pattern against the Gram positive organisms. For the most common pathogen, Klebsiella pneumoniae, apart from colistin(100%), meropenem (89%) followed by amikacin (81%) and imepenem (80%) showed the best sensitivity patterns. Pseudomonas showed a similar preference for meropenem (90%) and amikacin (81%) apart from colistin (100%). Staphylococcus aureus with good sensitivity for linezolid (100%) , Streptococcus pneumoniae (Ceftriaxone 100%) and Moraxella catarrhalis (3^rd gen cephaosporins) were the other results obtained.

Discussion:

In hospital setting, empirical management for cases of CAP should be based on local bacteriological profile. The present study has shown K.pneumoniae as the most common pathogen in hospitalized patients with CAP. Choosing the proper antibiotics as initial empiric therapy & later streamlining as per the culture sensitivity pattern is critical in outcome of CAP. Patients with signs of shock should empirically be started with carbapenems along with a aminoglycoside or quinolones whichever is clinically feasible. If patient is relatively stable, instead of carbapenems, beta-lactams/beta lactamase inhibitors are advised. 3^rd generation cephalosporin together with quinolones is also a good alternative for the stable CAP cases. Later on based on sensitivity reports, the antibiotics are to be de-escalated. Indiscriminate use of carbapenams can be avoided in these patients, since beta-lactams/beta lactamase inhibitors also caters to the need, leading to better antibiotic stewardship. Colistin is a restricted antibiotic and should only be reserved for hospital acquired pneumonia cases and are in no way justified for CAP.

Conclusion:

Interestingly we find klebsiella to be most common pathogen (43.2%), followed by  Pseudomonas aeruginosa (23%; n= 44)  and Staphylococcus aureus (10%; n= 19). Esherichia coli (7.8%;n= 15), Streptococcus pneumonaie (3.1%; n= 6) and Moraxella catarrhalis (2%; n=4) were the other organisms. These changing trends needs to be keep in mind while choosing empirical coverage in this area.

References:

[1] Alaka Deshpande. Epidemiology of community acquired pneumonia. JAPI. 2012; 60: S6.

[2] Mandell LA. Update on community-acquired pneumonia. New pathogens and new concepts in treatment. Postgard Med. 2005; 118:35-6.

[3] Mandell L A, Wunderink R G, Anzueto A, Bartlett J G, Campbell G D, Dean N C, et al. Infectious diseases society of america/american thoracic society consensus guidelines on them management of community-acquired pneumonia in adults. CID. 2007; 44: S27–72.

[4]  Mandella LA. Epidemiology and etiology of community-acquired    pneumonia. Infect Dis Clin North Am. 2002; 18:761-76.

[5] Al-Ali MK, Batchoun RG, Al-Nour TM. Etiology of community-acquired pneumonia in hospitalized patients in Jordan. Saudi Med J. 2006; 27:813-6.

[6] Reechaipichitkul W, Lulitanond V, Tantiwong P, Saelee R, Pisprasert V. Etiologies and treatment outcomes in patients hospitalized with community-acquired pneumonia at Srinagarind Hospital, KhonKaen, Thailand. Southeast Asian J Trop Med Public Health. 2005; 36:156-61.

[7] Niederman MS. Review of treatment guidelines for community-acquired pneumonia. Am J Med. 2004: 117 Suppl 3A:51-7.

[8] Riquelme O R, Riquelme O M, Riquelme O M, Rioseco Z ML, Gomez M V, Gil D R. Etiology and prognostic factors of community-acquired pneumonia among adult patients admitted to a regional hospital in Chile. Rev Med Chil. 2006; 134: 597-605.

[9] Bansal S, Kashyap S, Pal LS, Goel A. Clinical and bacteriological profile of community-acquired pneumonia in Shimla, Himachal Pradesh. Indian J Chest Dis Allied Sci. 2004; 46:17-22.

[10] Djukanovic R, Sterk PJ, Fahy JV, Hargreave FE. Standardised methodology of sputum induction and processing. EurRespir J. 2002; 20: 19-39.

Author:

1. Dr. Vicky Lahkar, (Consultant, Microbiologist, Narayana Superspeciality Hospital, Guwahati)
2. Dr. Apurba Kumar Borah (Consultant & HOD, CCEM, Narayana Superspeciality Hospital, Guwahati)

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